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Vinegar Ingestion at Bedtime Moderates Waking Glucose Conce... http://care.diabetesjournals.org/content/30/11/2814.full Vinegar Ingestion at Bedtime Moderates Waking Glucose Concentrations in Adults With Well-Controlled Type 2 Diabetes Andrea M. White, PHD and Carol S. Johnston, PHD + Author Affiliations Address correspondence and reprint requests to Dr. Carol S. Johnston, 7001 E. Williams Field Rd., Mesa, AZ 85212. E-mail: [email protected] Given the importance of maintaining acceptable blood glucose concentrations, there is much interest in identifying foods and diet patterns that will help individuals with diabetes manage their condition. Based on previous data indicating that vinegar ingestion at mealtime reduces postprandial glycemia (1–4), the aim of this pilot study was to examine whether vinegar ingestion at bedtime reduces the next-morning fasting glucose concentration in individuals with type 2 diabetes. RESEARCH DESIGN AND METHODS— Four men and seven women (aged 40–72 years) diagnosed with type 2 diabetes (by a physician) who were not taking insulin completed the study. Participants provided a clinically determined A1C reading from a recent (<2 months) blood analysis. All participants gave written informed consent, and the study was approved by the institutional review board at Arizona State University. Participants maintained 24-h diet records for 3 days and measured fasting glucose at 0700 h for 3 consecutive days with a calibrated glucometer before the start of the study. Participants were instructed to continue usual prescription medication use during the study. Utilizing a randomized crossover design with a 3- to 5-day washout period between treatments, participants followed a standardized meal plan for 2 days, consuming either 2 Tbsp apple cider vinegar or water at bedtime with 1 oz cheese (8 g protein, 1 g carbohydrate, and 1.5 g fat). The standardized meal plan was designed to reflect the individual's typical diet. Participants were instructed to record all foods and beverages ingested during each 2-day treatment period. Fasting glucose was recorded with a calibrated glucometer by each participant during the trial: at baseline (day 0) and day 2 at 0700 h. These results were downloaded by the research staff from each participant's glucometer memory. A multivariate repeatedmeasures ANOVA test with body weight as a covariate was used to determine a significant time-by-treatment effect using SPSS (version 14 for Windows; SPSS, Chicago, IL). RESULTS— The duration of diabetes averaged 4.9 ± 1.0 years for the participants, and 73% of participants (8 of 11) used prescription hypoglycemic agents during the study. Before the 2 initiation of the study, a BMI of 29.1 ± 1.2 kg/m , a typical fasting glucose of 7.6 ± 0.3 mmol/l, and an A1C of 6.7 ± 0.2% were recorded for the participants. Participants complied with the dietary protocol as indicated by the diet records maintained during the study; hence, food intake for the two treatment periods was identical within subjects. Fasting glucose was reduced 0.15 mmol/l (2%) and 0.26 mmol/l (4%) for the placebo and vinegar treatments, respectively (time-by-treatment effect, P = 0.033) (Fig. 1). Closer examination of the data revealed that the vinegar treatment was particularly effective for the participants with a typical fasting glucose >7.2 mmol/l; in these individuals (n = 6), fasting glucose was reduced 6% compared with a reduction of 0.7% in those participants with a typical fasting glucose <7.2 mmol/l (n = 5). CONCLUSIONS— These data suggest that vinegar ingestion at bedtime may favorably impact waking glucose concentrations in type 2 diabetes. The antiglycemic effect of acetic acid, the active ingredient in vinegar, has been attributed to reduced starch digestion (5) and/or delayed gastric emptying (6). Neither of these proposed mechanisms likely explains the effects noted herein; moreover, to our knowledge, this is the first report describing a hypoglycemic effect of vinegar apart from mealtime. Fushimi et al. (7,8) have published a series of trials in rats demonstrating that acetic acid alters hepatic and skeletal glucose metabolism. These 1 of 3 2/21/10 10:06 AM Vinegar Ingestion at Bedtime Moderates Waking Glucose Conce... http://care.diabetesjournals.org/content/30/11/2814.full investigations show that acetic acid feeding (0.2 acetic acid/100 g diet) reduced xylulose5-phosphate accumulation in liver and phosphofructokinase-1 activity in skeletal muscle —metabolic changes consistent with reduced glycolysis and the promotion of glycogen synthesis. Hence, acetic acid may possibly alter the glycolysis/gluconeogenic cycle in liver, which may benefit diabetic individuals with metabolic disturbances contributing to a prebreakfast rise in fasting glucose (also known as the “dawn phenomenon”) (9). Reductions in fasting glucose of the magnitudes noted in this study (4–6%) are less than that observed in trials examining the efficacy of pharmaceutical hypoglycemic agents for inadequately controlled diabetes. In these trials, pretrial A1C values averaged 7.8–8.8%, and fasting glucose concentrations were reduced 10–15% by long-term drug therapy (10–12). In comparison, the diabetic condition of our subjects was well controlled (A1C 6.7 ± 0.2%). Notably, although 72% of our subjects regularly used hypoglycemic medications and continued their medication use during the study, the vinegar treatment significantly impacted fasting glucose. In individuals with early diabetes (A1C <6.3%) or well-controlled diabetes (A1C 6.8–7.0%), pharmaceutical interventions had a more moderate effect, reducing fasting glucose 3–6% (13,14). The control cheese plus water treatment reduced fasting glucose 2% (P = 0.928), whereas the cheese plus vinegar treatment reduced fasting glucose 4% (P = 0.046). We cannot rule out the possibility of a synergistic effect for cheese and vinegar. Based on our previous work, we felt that the subjects needed a small amount of food to take with the vinegar for ease of application. Fasting hyperglycemia in type 2 diabetes has been related to an intrahepatic malfunction that increases overall hepatic glucose output, perhaps the inhibition of glycogen synthesis (15). In type 2 diabetes, dietary protein has a minimal effect on glycemia, even though gluconeogenesis is increased (16,17). Amino acids from cheese may provide glucogenic substrates, which in the presence of insulin convert to glycogen (18,19), a scenario that may benefit individuals with type 2 diabetes. We were unable to find research investigating a role for nighttime snacks in managing waking hyperglycemia in type 2 diabetes; our data suggest that this possibility should be explored. Although this study is limited by the small sample size (n = 11), the within-subject design reduced error variance due to individual differences. Also, renal function and a detailed history of medication use were not assessed in this study and may have impacted these results. Vinegar is widely available, it is affordable, and it is appealing as a remedy, but much more work is required to determine whether vinegar is a useful adjunct therapy for individuals with diabetes. Investigations are needed to study the mechanisms by which vinegar alters postprandial glycemia and fasting glucose and to examine the efficacy of vinegar ingestion in individuals with inadequately controlled diabetes. Figure 1— Fasting glucose concentrations at baseline and on day 2 of placebo or vinegar treatment in type 2 diabetic patients (n = 11). Values are means ± SE. The P value represents the time-by-treatment effect (multivariate repeatedView larger version: In this page In a new window measures ANOVA test). Footnotes Published ahead of print at http://care.diabetesjournals.org on 21 August 2007. DOI: 10.2337/dc07-1062. A table elsewhere in this issue shows conventional and Système International (SI) units and conversion factors for many substances. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C Section 1734 solely to indicate this fact. Accepted August 13, 2007. 2 of 3 2/21/10 10:06 AM Vinegar Ingestion at Bedtime Moderates Waking Glucose Conce... http://care.diabetesjournals.org/content/30/11/2814.full Received June 4, 2007. DIABETES CARE References 1. Ebihara K, Nakajima A: Effect of acetic acid and vinegar on blood glucose and insulin responses to orally administered sucrose and starch. Agric Biol Chem 52: 1311–1312, 1988 2. Brighenti F, Castellani G, Benini L, et al: Effect of neutralized and native vinegar on blood glucose and acetate responses to a mixed meal in healthy subjects. Eur J Clin Nutr 49: 242–247, 1995 Medline 3. Sugiyama M, Tang AC, Wakaki Y, et al: Glycemic index of single and mixed meal foods among common Japanese foods with white rice as a reference food. Eur J Clin Nutr 57: 743–752, 2003 Medline 4. Johnston CS, Buller AJ: Vinegar and peanut products as complementary foods to reduce postprandial glycemia. J Am Diet Assoc 105: 1939–1942, 2005 Medline 5. Ogawa N, Satsu H, Watanabe H, et al: Acetic acid suppresses the increase in disaccharidase activity that occurs during culture of caco-2 cells. J Nutr 130: 507–513, 2000 Abstract/FREE Full Text 6. Liljeberg H, Bjorck I: Delayed gastric emptying rate may explain improved glycaemia in healthy subjects to a starchy meal with added vinegar. Eur J Clin Nutr 52: 368–371, 1998 CrossRef Medline Web of Science 7. Fushimi T, Tayama K, Fukaya M, et al:Acetic acid feeding enhances glycogen repletion in liver and skeletal muscle of rats. J Nutr 131: 1973–1977, 2001 Abstract/FREE Full Text 8. Fushimi T, Tayama K, Fukaya M, et al: The efficacy of acetic acid for glycogen repletion in rat skeletal muscle after exercise. Int J Sports Med 23: 218–222, 2002 Medline 9. Monnier L, Colette C, Dunseath GJ, et al: The loss of postprandial glycemic control precedes stepwise deterioration of fasting with worsening diabetes. Diabetes Care 30: 263–269, 2007 Abstract/FREE Full Text 10. Home PD, Jones NP, Pocock SJ, et al: Rosiglitazone RECORD study: glucose control outcomes at 18 months. Diabet Med 24: 626–634, 2007 CrossRef Medline 11. Perriello G, Pampanelli S, Di Pietro C, et al: Comparison of glycaemic control over 1 year with pioglitazone or gliclazide in patients with type 2 diabetes. Diabet Med 23: 246–252, 2006 CrossRef Medline Web of Science 12. Derosa G, Gaddi AV, Piccinni MN, et al: Differential effect of glimepiride and rosiglitazone on metabolic control of type 2 diabetic patients treated with meformin: a randomized, double-blind, clinical trial. Diabetes Obes Metab 8: 197–205, 2006 CrossRef Medline Web of Science 13. Eguchi K, Tomizawa H, Ishikawa J, et al: Comparison of the effects of pioglitazone and metformin on insulin resistance and hormonal markers in patients with impaired glucose tolerance and early diabetes. Hypertens Res 30: 23–30, 2007 Medline 14. Jung CH, Rhee EJ, Kim ER, et al: Comparison of the alteration of the concentration of C-peptide in 24-h urine according to the combination patterns of hypoglycemic agents in type 2 diabetes patients. Diabetes Res Clin Prac. 2007, DOI: 10.1016/j.diabres.2007.01.059 [Epub ahead of print] 15. Jenssen T, Nurjhan N, Consoli A, et al: Failure of substrate-induced gluconeogenesis to increase overall glucose appearance in normal humans. J Clin Invest 86: 489–497, 1990 Medline Web of Science 16. Gannon MC, Nuttall JA, Damberg G, et al: Effect of protein ingestion on the glucose appearance rate in people with type 2 diabetes. J Clin Endocrinol Metab 86: 1040–1047, 2001 Abstract/FREE Full Text 17. Krebs M, Brehm A, Krssak M, et al: Direct and indirect effects of amino acids on hepatic glucose metabolism in humans. Diabetologia 46: 917–925, 2003 CrossRef Medline Web of Science 18. Franz MJ: Protein: metabolism and effect on blood glucose levels. Diabetes Educ 23: 643–646, 1997 FREE Full Text 19. Edgerton DS, Cardin S, Emshwiller M, et al: Small increases in insulin inhibit hepatic glucose production solely caused by an effect on glycogen metabolism. Diabetes 50: 1872–1882, 2001 Abstract/FREE Full Text 3 of 3 2/21/10 10:06 AM